ESPE Abstracts

Background: Translational research has provided evidence of autonomic nervous system (ANS) interactions with cytokines and gut hormones. In the gastrointestinal track, the crosstalk of the stimulated vagus nerve with immune cells enhances the cholinergic tone. In obesity, on the other hand, hyperinsulinemia and hyperleptinemia induce ANS activation.

Aim: To synthesize literature results exploring links among the autonomic nervous system, gut hormones, immune factors, and pancreatic β-cell function.

Methods: Literature search in PUBMED, Scopus.

Results: A study in animal models showed an association between ANS and inflammatory markers (Matteoli & Boeckxstaen, 2013). In obese patients with and without diabetes type 2, an association between ANS and inflammatory factors with, independent of BMI or fat loss, after bariatric surgery, was observed (Casellini 2016). Importantly, a meta-analysis after bariatric surgery that evaluated the interaction of ANS and insulin resistance, suggested a link betweenthe ANS, the gut, and pancreatic islet β-cells (Geronikolou 2017a). A separate interactions network within the so-termed “Obesidome” has been created to explore this interplay (Geronikolou 2017b). Our results show that there is an intricate communication network between the nervous and immune systems and that this interplay could be involved in the regulation of the immune response. TGF-beta and thymic stromal lymphopoietin produced by the GI enterocytes and/or immune cells may contribute to the maintenance of immune homeostasis. The interactions between the autonomic, inflammatory, and hormonal biomarkers and their encoding genes revealed that JAK2 serves as a key hub for leptin and insulin activity, thus, providing the basis for further investigation.

Conclusions: The autonomic nervous and immune system interplay may provide an independent mechanism of energy homeostasis warranting future research.